This chapter is divided into three major sections. In the first section, a model of Campylobacter jejuni-mediated enteritis is presented. The second section presents a general overview of the organism's pathogenic mechanisms and virulence determinants. Finally, in the third section, various aspects of C. jejuni-host cell invasion and protein secretion are discussed. Specifically, in the third section C. jejuni protein export via the flagellar type III secretion system (T3SS), the development of an assay to identify C. jejuni secreted proteins, the evolutionary relatedness of the flagellum and virulence T3SS, and the putative roles of C. jejuni secreted proteins in disease, are discussed. Although much remains unknown regarding the identity and functional characteristics of the proteins exported via the flagellar apparatus, the chapter highlights evidence supporting the proposal that these proteins contribute to C. jejuni-mediated enteritis. Motility, adherence, invasion, protein secretion, intracellular survival, and toxin production may contribute to the pathogenicity of a given C. jejuni strain. C. jejuni nonmotile strain can be either secretion positive (i.e., the flaAflaB+ mutant) or secretion negative (i.e., the flaAflaB mutant), and the ability of the bacterium to secrete proteins can result in an increase in its invasive potential. Although these data helped clarify the relationship between C. jejuni motility, secretion, and host cell invasion, the significance of protein secretion and host cell invasion in C. jejuni-mediated gastroenteritis was not known.

Adherence, protein secretion, and invasion are a few of the C. jejuni virulence attributes that contribute to acute infection. As depicted, bacterial colonization of the intestinal tract can occur by different routes. Several virulence attributes may stimulate the host inflammatory response and in turn promote additional bacteria–host cell interactions. Other factors (not listed) are also capable of triggering the host inflammatory response. The dotted line represents the possibility that secreted proteins may enhance the cytokine response.

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Figure 2.

Adherence, protein secretion, and invasion are a few of the C. jejuni virulence attributes that contribute to acute infection. As depicted, bacterial colonization of the intestinal tract can occur by different routes. Several virulence attributes may stimulate the host inflammatory response and in turn promote additional bacteria–host cell interactions. Other factors (not listed) are also capable of triggering the host inflammatory response. The dotted line represents the possibility that secreted proteins may enhance the cytokine response.

C. jejuni type III secretion system (T3SS) is the flagellum that secretes the Campylobacter secreted proteins (Csp). A subset of the Csps, termed the Campylobacter invasion antigens (Cia), are required for maximal invasion. Both the Csp and Cia proteins harbor nonconsensus secretion signals, which are required for export.

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Figure 4.

C. jejuni type III secretion system (T3SS) is the flagellum that secretes the Campylobacter secreted proteins (Csp). A subset of the Csps, termed the Campylobacter invasion antigens (Cia), are required for maximal invasion. Both the Csp and Cia proteins harbor nonconsensus secretion signals, which are required for export.

72. Newell,D. G.,, H.McBride, and, J. M.Dolby.1985a.Investigations on the role of flagella in the colonization of infant mice with Campylobacter jejuni and attachment of Campylobacter jejuni to human epithelial cell lines.J. Hyg. (Lond.)95:217–227.